MicroRNA-593-3p regulates insulin-promoted glucose consumption by targeting Slc38a1 and CLIP3

    1. Huajun Fan2
    1. 1Department of Otorhinolaryngology - Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China
    2. 2Department of Plastic Surgery, Renmin Hospital of Wuhan University, Wuhan, China
    1. Correspondence should be addressed to Z Tao or Z Zhu; Email: taozezhang{at}hotmail.com or zyzhu{at}whu.edu.cn


    Insulin plays an important role in the regulation of glucose metabolism. However, the molecular mechanisms involved are not entirely clarified. In this context, we found that miR-593-3p negatively regulates insulin-regulated glucose metabolism in hepatocellular carcinoma HepG2 and Bel7402 cells. We then identified Slc38a1 and CLIP3 as novel targets of miR-593-3p. Further studies demonstrated that Slc38a1 and CLIP3 mediate insulin-regulated glucose metabolism. Interestingly, we also demonstrated that miR-593-3p expression was negatively associated with Slc38a1 and CLIP3 expression in insulin-treated HepG2 cells, and insulin-induced Slc38a1 and CLIP3 expression via downregulation of miR-593-3p. Taken together, this study indicates that inhibition of miRNA-593-3p by insulin promotes glucose metabolism through the regulation of Slc38a1 and CLIP3 expression, and provides a new insight into the role and mechanism of insulin-induced glycolysis.

    • Received 18 August 2016
    • Accepted 7 September 2016
    • Made available online as an Accepted Preprint 9 September 2016
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